Flashcards in Drugs and the CVS Deck (11):
What causes Arrhythmias?
Ectopic pacemaker activity due to damaged myocardium.
What is an after-depolarisation and what is a common cause of them?
Depolarisation after the action potential prolonging the action potnetial, these are common with high intracellular Ca++
What is an early after-depolarisation?
Depolarisation at the end of the action potential
What is a re-entry loop and what can they cause?
Re-entry loops are due to incomplete or unidirectional blocks of electrical activity that set up a circuit, = several re-entry loops can lead to AF.
Name 4 categories of anti-arrhythmia drugs.
Blockage of voltage gated sodium channels when they are in the open or inactive stage and dissociate rapidly e.g. lidocaine which helps prevent after depolarisations.
Beta-adrenoreceptor antagonists such as atenolol and propranolol these slow the heart reducing oxygen demand preventing ventricular arrhythmias after an MI, they also slow conduction at AV node so good for supraventricular tachycardia.
K+ channel blockers prolong action potential to slow the heart (actually pro arrhythmic so not used except for amiodarone).
Ca++ channel blockers such as Verapamil which slows conduction at AV node and decreases force of contraction as well as some coronary and peripheral dilation (some of these Ca drugs only work on vascular smooth muscle and are called dihydropyridines).
How does Adenosine act as an anti-arrhythmia
Adenosine can be administered intravenously – this enhances K+ conductance hyperpolarising cells blocking conduction temporarily to bring back to sinus rhythm.
What is Heart Failure
Adequate filling pressure but inadequate cardiac output.
How do we pharmacologically treat Heart failure?
Increase contractility – cardiac glycosides block Na+/K+ ATPase pump resulting in build-up of Na+ and so Na/Ca exchanger doesn’t work as well so more Ca stored in the SR (also increases vagal activity of heart so slows heart down)
Beta agonists such as Dobutamine which increase rate and contractility of the heart.
Reduce the workload – ACE inhibitors – Angiotensin 2 acts on the kidneys to increase Na+ and water uptake (increase volume of blood = increase output) and is also a vasoconstrictor.
Organic nitrates - vasodilation to increase blood flow to ischaemic areas and venodilation reduceing pre load.
How would we pharmacologically treat Hypertension?
BP = flow x resistance so BP = CO x TPR – so must decrease CO and TPR. Diuretics, ACE-inhibitors, beta blockers, some Ca++ channel blockers and Alpha 1 antagonists.
How would we pharmacologically treat Angina
Reduce the workload of the heart and increase blood flow to the heart – Beta antagonist, Ca++ channel blockers and organic nitrates.